The protocol proposes to use established methodology for assessing upper airway resistance and respiratory drive during wakefulness and sleep in order to explain the apparent paradox between the known independent risk factor of cigarette smoking for obstructive sleep apnea, and the fact that nicotine is a respiratory simulant which may also reduce upper airway resistance and has even been suggested as a method of treatment of obstructive sleep apnea. The hypotheses being tested are 1) nicotine will increase respiratory drive as measured by the rate of inspiratory change in esophageal pressure and by responses to hypercapnia and to isocapnic hypoxia, 2) the irritants contained in cigarette smoke will tend to increase upper airway resistance primarily through increased nasal resistance, and 3) the combination of increased inspiratory effort with increased upper airway resistance will cause instability of the upper airway and lead to more snoring and more obstructive events during sleep in the smoking condition.